A subset of tumors might display significant adaptive resistance after post-combined modality therapy, manifested by an active immune microenvironment characterized by increased CD8 infiltration and IFNγ, leading to the compensatory induction of multiple checkpoints, including PD-1, PD-L1, CTLA-4, LAG-3, and IDO, to prevent tumor cell death [33,34]. This evidence concerns the gene CTLA4 and neoplasm.